Methemoglobinemia epidemiology and demographics
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Template:Aksiniya K. Stevasarova, M.D.
Overview
Congenital (Hereditary) Methemoglobinemia
There are three main congenital conditions that lead to methemoglobinemia:
1. Cytochrome b5 reductase deficiency and pyruvate kinase deficiency
3. Presence of abnormal hemoglobin (Hb M)
Acquired or Acute Methemoglobinemia
Most common cause include different oxidant drugs, toxins or chemicals
Epidemiology and Demographics
The incidence of congenital methemoglobinemia in the United States is very low.
Age
- Patients of all age groups may develop methemoglobinemia.
- The acquired methemoglobinemia is a rare disease that tends to affect infants and people exposed to local anesthetics during medical procedures.
- Infants, particularly those younger than 4 months are most susceptible to methemoglobinemia. This is due to the fact that the NADH methemoglobin reductase activity and concentration (the main protective enzyme against oxidative stress) is not fully mature in infants.
Gender
- The incidence of the congenital methemoglobinemia is the same for both genders as both cytochrome b5 reductase deficiency and pyruvate kinase deficiency are autosomal recessive diseases and the Hb M has autosomal dominant pattern of inheritance.
- The incidence of ([G6PD]] deficiency is is greater in males as this condition has X-linked pattern of inheritance. There is no racial predilection to Methemoglobinemia.
Developed Countries
- There is no racial predilection to methemoglobinemia.
- In developed countries, the incidence of acquired methemoglobinemia is higher in developing countries when people are exposed to local anesthetics during various medical procedures.
- The majority of cytochrome b5 reductase deficiency cases are found among some Native American tribes like Navajo [1] and Athabaskan Alaskans, and the Yakutsk people in Siberia. [2]
Developing Countries
- The highest prevalence of G6PD deficiency is observed in the malaria-endemic regions: Sub-Saharan Afria, West Asia and Arabian Peninsula, as well as in people of Mediterranean descent. Howes RE1, Dewi M, Piel FB, Monteiro WM, Battle KE, Messina JP, Sakuntabhai A, Satyagraha AW, Williams TN, Baird JK, Hay SI. pmid=24228846 }}</ref> [3] [4]
- ↑ {{J Pediatr. 1964 Dec;65:928-31. HEREDITARY METHEMOGLOBINEMIA DUE TO DIAPHORASE DEFICIENCY IN NAVAJO INDIANS. BALSAMO P, HARDY WR, SCOTT EM. pmid=14244100}}
- ↑ {{J Pediatr Hematol Oncol. 2017 Jan;39(1):42-45. Enzymopenic Congenital Methemoglobinemia in Children of the Republic of Sakha (Yakutia). Burtseva TE1, Ammosova TN, Protopopova NN, Yakovleva SY, Slobodchikova MP. pmid=27879543 }}
- ↑ {{ Adv Parasitol. 2013;81:133-201. doi: 10.1016/B978-0-12-407826-0.00004-7. G6PD deficiency: global distribution, genetic variants and primaquine therapy. Howes RE1, Battle KE, Satyagraha AW, Baird JK, Hay SI.pmid=23384623}}
- ↑ Template:Pmid=1917622